ArticleNeuron2008
Balancing between adaptive and maladaptive cellular stress responses in peripheral neuropathy.
Article in Neuron, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed.
- De novo variants in EMC1 lead to neurodevelopmental delay and cerebellar degeneration and affect glial function in Drosophila.Human molecular genetics · 2022Article
- Biology in balance: human diploid genome integrity, gene dosage, and genomic medicine.Trends in genetics : TIG · 2022Review
- El-Hattab-Alkuraya syndrome caused by biallelic WDR45B pathogenic variants: Further delineation of the phenotype and genotype.Clinical genetics · 2022Article
- Effects of a solid lipid curcumin particle formulation on chronic activation of microglia and astroglia in the GFAP-IL6 mouse model.Scientific reports · 2020Article
- ZIKV infection activates the IRE1-XBP1 and ATF6 pathways of unfolded protein response in neural cells.Journal of neuroinflammation · 2018Article
- Curcumin facilitates a transitory cellular stress response in Trembler-J mice.Human molecular genetics · 2013Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Point mutations in "myelin genes" result in a spectrum of inherited demyelinating neuropathies. The understanding of the pathomechanisms by which these mutations produce phenotypes remains limited. In this issue of Neuron, Wrabetz and colleagues report that the unfolded protein response (UPR) is responsible for demyelination in a Charcot-Marie-Tooth disease type 1B (CMT1B) mouse model. Deletion of the UPR mediator transcription factor CHOP completely rescues the motor deficit and ameliorates the neuropathy phenotype.
Indexed as
Identifiers
18255024What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.